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 Table of Contents  
CASE REPORT
Year : 2022  |  Volume : 17  |  Issue : 1  |  Page : 132-136

Acquired melanocytic nevus in head-and-neck region – A case series


1 Department of Oral and Maxillofacial Pathology, MGM's Dental College and Hospital, MGMIHS, Navi Mumbai, Maharashtra, India
2 Department of Oral and Maxillofacial Surgery, MGM's Dental College and Hospital, MGMIHS, Navi Mumbai, Maharashtra, India

Date of Submission07-Jul-2021
Date of Decision21-Dec-2021
Date of Acceptance23-Feb-2022
Date of Web Publication25-Jul-2022

Correspondence Address:
Dr. Jigna Pathak
Department of Oral and Maxillofacial Pathology, MGM's Dental College and Hospital, MGMIHS, Navi Mumbai, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jdmimsu.jdmimsu_266_21

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  Abstract 


Acquired melanocytic nevus (AMN) is the most common benign proliferative lesion of melanocytes occurring on the skin after birth. Nevi can occur under the genetic influence or certain environmental factors. Histopathologically, they are categorized as an intradermal, compound, and junctional nevus. The significance of nevi lies in their relation to melanoma with malignant transformation rate being 4%–9%. We, hereby present an institutional case series of AMN in the head-and-neck region.

Keywords: Head-and-neck region, melanocytic nevus, melanoma


How to cite this article:
Pathak J, Sarkate P, Gandevivala A, Hosalkar R, Swain N. Acquired melanocytic nevus in head-and-neck region – A case series. J Datta Meghe Inst Med Sci Univ 2022;17:132-6

How to cite this URL:
Pathak J, Sarkate P, Gandevivala A, Hosalkar R, Swain N. Acquired melanocytic nevus in head-and-neck region – A case series. J Datta Meghe Inst Med Sci Univ [serial online] 2022 [cited 2022 Aug 18];17:132-6. Available from: http://www.journaldmims.com/text.asp?2022/17/1/132/352225




  Introduction Top


An acquired melanocytic nevus (AMN) is a benign proliferative lesion of melanocytes that occurs on the skin after birth. AMN is the most common type of nevus.[1] Approximately 20% of nevi occur in the head-and-neck region with intradermal nevus (common mole) being the most common type.[2] The emergence of nevi is under strong genetic control, whereas environmental exposures affect the mean number of nevi. The amount of sun exposure is the most important environmental risk factor for nevus development, particularly in early childhood.[3] Therefore, preventive measures for nevus and melanoma development should target young children and adolescents.[4]

The pathogenesis of AMN is still not clear, and the origin of nevus cells has not been clarified. Common nevi typically harbor BRAF V600E mutations (~85%) with neuroblastoma ras viral oncogene homolog NRAS mutations present in a minority of cases. The BRAF mutation affects one of two alleles in every melanocyte of the nevus, indicating that a nevus is the result of a clonal outgrowth of a single melanocyte that acquired the BRAF V600E mutation.[5] AMN can be pathologically divided into the junctional, compound, and intradermal nevi according to the site of the nevus cell nests.[6] AMN is usually treated by excision or by laser. Junctional nevi respond to Q-switched/normal mode pigment lasers, whereas for the compound and dermal nevi, pulsed ablative laser (CO2/Er: YAG) may be needed. If surgical excision is employed, a wide margin and proper depth must be ensured.[7] The main pathological significance of nevi lies in their relation to melanoma. They may be simulants of melanoma, potential precursors of melanoma, or markers of risk for developing melanoma. The incidence of malignant transformation in naevi is 4%–9%.[8] We, hereby present an institutional case series of AMN in the head-and-neck region. With the primary objective of evaluating the clinical and histopathological features of all the institutional cases reported and diagnosed as AMN. And also compare the clinical and histopathological features of all the institutional cases of AMN with the reported cases.


  Case Report Top


We report a series of 6 cases of nevi reported to the department of oral pathology and microbiology with a chief complaint of growth and poor aesthetics due to the presence of mole. A total of 6 cases comprising 3 male and 3 female patients in the age range of 20–50 years are presented. Written patient consents were obtained for history, biopsy, and subsequent surgery. Clinical presentation of all the cases of AMN in the head-and-neck region are elaborated in [Table 1] and also shown in [Figure 1]. The primary goal of management is to remove the risk of malignant transformation while minimizing functional deformity and improving cosmetics. After clinical examination, all the patients were referred to the department of oral surgery for excisional biopsy as complete excision of the nevus with clear deep surgical margins can effectively reduce or eliminate the risk of malignant transformation. Further processing and histopathological examination of each biopsy specimen were done in the department of Oral Pathology and Microbiology [Table 1] and [Figure 2]. The patients were kept on 6 months of follow-up for 3 years. No recurrence or any other complications were observed.
Table 1: Clinicopathological characteristics of acquired melanocytic nevi in the head-and-neck region visiting the dental institution

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Figure 1: Clinical photograph of the six cases of head and neck nevi (yellow arrow marks)

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Figure 2: (a and b) Microphotograph of compound nevus showing pigmented nevus cells extending from dermo-epidermal junction into dermis (yellow-dotted line, H and E, ×40) with Abtropfung (dropping off) effect (H and E, ×100); (c and d) intradermal nevus deep within the dermis (yellow line, H and E, ×40) with type B nevus cells (H and E, ×100)

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  Discussion Top


Acquired melanocytic nevi (AMN) also referred to as “signature nevi,” is a common, largely acquired condition resulting from the benign proliferation of nevus cells.[7] Cells comprising a melanocytic nevus are known as “nevus cells” or “naevomelanocytes.” Nevus cells (Latin for “maternal impression” or “birthmark”) are melanocytes that have lost their long dendritic processes due to an adaptive response associated with the formation of nests of cells.[4] There are transitional stages in the life cycle of nevi, which are believed to start out as junctional nevi, then become compound nevi, and after having become intradermal nevi, undergo involution.[9] The evolution and regression of nevi correlate with their histologic appearance. The junctional and compound proliferation of nevus cells is present in children, whereas intradermal nevi, by contrast, are most unusual in the first decade of life.[10] Contrary to this, in the present case series, compound nevi were seen in older individuals compared to intradermal nevi which were seen in young adults.

Acquired nevi are thought to undergo maturation from junctional to the compound to intradermal forms due to “Abtropfung” (“dropping off”) of nevus cells, but this concept has been questioned with upward migration being proposed.[11] There are three pathophysiological theories of the development of nevi-Unna's Abtropfung (“trickling down”) theory, Masson's dual origin theory, and Cramer's Hochsteigerung (“upward climbing”) theory which is illustrated in [Figure 3].[12] Out of these, the Abtropfung theory is the most widely accepted theory. According to this concept, melanocytic nevus cells are derived from epidermal melanocytes (EMC) and gradually migrate into the dermis, during which time junctional, compound, and intradermal nevi are sequentially formed. However, Masson and Cramer proposed that nevus cells are derived from dermal stem cells (DSCs). There is a possibility that Schwann cells produce DSCs and then form melanocytic nevi.[12] Although morphologically nevus cells differ from melanocytes as depicted in [Table 2], electron microscopically, they appear similar to them, and thus, it is concluded that nevus cells are variants of melanocytes[9] Wang et al.[12] stated that intradermal nevi can occur in children and are not always evolved from junctional nevi indicating that melanocytic nevi may have other cellular origins, most likely DSCs and hair follicle stem cells (HFSC).[12] Thus, nevus cells are thought to have several cellular origins which are depicted diagrammatically in [Figure 4]. Furthermore, it is hypothesized that EMCs may undergo dedifferentiation during downward migration from the epidermis and show characteristics of transformation to dermal tissue.
Table 2: Comparison between melanocytes and nevus cells

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Figure 3: Illustration of different origins of nevus cells and associated immunohistochemical markers

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Figure 4: Illustration of different theories of oral nevi development

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The clinicopathological comparison between the junctional, compound, and intradermal nevi is elaborated in [Table 3] and [Table 4] [3] with different variations in the morphology of nevus cells listed in [Table 5].[1] Our case series was histopathologically categorized on the basis of the above. However, in our case series, 4 out of 6 cases were of compound nevus, and the remaining 2 were intradermal nevus are illustrated in [Figure 2]. Immunohistochemical markers studied in various nevi are illustrated in [Figure 4]. In a study, it was seen that intradermal nevi were strongly positive for nestin, whereas junctional nevi were positive for E-cadherin, DDR-1, and alpha-6 integrin. This supports the origin of intradermal nevi from DSC and junctional nevus from the EMC. Therefore, the question remains of whether there is an upward growth pattern, i.e., can DSCs produce an intradermal nevus, continue to grow upward, and transform into a compound nevus and eventually a junctional nevus?[13]
Table 3: Clinical comparison of the junctional, compound, and intradermal nevus

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Table 4: Histological comparison of the junctional, compound, and intradermal nevus

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Table 5: Variable morphology of nevus cells

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Nevi are risk markers, simulants, and potential precursors of malignant melanoma besides posing a cosmetic problem. In a recent study, 2.3% of clinically diagnosed benign nevi were microscopically diagnosed as malignant tumors, either melanomas or basal or squamous cell carcinomas.[14] The present case series showed no features of malignancy when diagnosed histopathologically and also no recurrence on a follow-up period of 3 years.


  Conclusion Top


AMN may have a multicellular origin. Although Abtropfung is a more common pattern (junctional to a compound to intradermal nevi), there is a possibility that nevi can grow in an upward direction from the dermis (intradermal) toward the epidermis (compound and junctional). Thus, we support the hypothesis that junctional nevi mostly have an EMC origin, whereas compound and intradermal nevi may be derived from DSC or HFSC.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patients have given their consent for their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published, and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Neville B, Damm DD, Allen C, Bouquot J. Textbook of Oral and Maxillofacial Pathology. 2nd ed., Ch. 10. Philadelphia: Elsevier Publication; 2009. p. 331-7.  Back to cited text no. 1
    
2.
Rajendran R, Sivapathasundharam B. Shafer's Textbook of Oral Pathology. 8th ed., Ch. 1. Philadelphia: Elsevier Publication; 2012. p. 19-22.  Back to cited text no. 2
    
3.
Sardana K, Chakravarty P, Goel K. Optimal management of common acquired melanocytic nevi (moles): Current perspectives. Clin Cosmet Investig Dermatol 2014;7:89-103.  Back to cited text no. 3
    
4.
Bauer J, Garbe C. Acquired melanocytic nevi as risk factor for melanoma development. A comprehensive review of epidemiological data. Pigment Cell Res 2003;16:297-306.  Back to cited text no. 4
    
5.
Yeh I. New and evolving concepts of melanocytic nevi and melanocytomas. Mod Pathol 2020;33:1-14.  Back to cited text no. 5
    
6.
Magana-Garcia M, Ackerman AB. What are nevus cells? Am J Dermatopathol 1990;12:93-102.  Back to cited text no. 6
    
7.
Sardana K. The science, reality, and ethics of treating common acquired melanocytic nevi (moles) with lasers. J Cutan Aesthet Surg 2013;6:27-9.  Back to cited text no. 7
[PUBMED]  [Full text]  
8.
Samaila MO, Adesiyun AG. Malignant transformation in pre-existing naevi. A review of two cases. Niger J Surg Res 2006;8:179-81.  Back to cited text no. 8
    
9.
Gundalli S, Kadadavar S, Singhania S, Kolekar R. Histopathological spectrum of benign melanocytic nevi – Our experience in a tertiary care centre. J Dermatol Online 2016;7:21-5.  Back to cited text no. 9
    
10.
Elder DE, Elenitsas R. Benign pigmented lesions and malignant melanoma. In: Lever's Histopathology of Skin. 9th ed. Philadelphia: Lippincott Raven; 2005. p. 715-804.  Back to cited text no. 10
    
11.
Worret WI, Burgdorf WH. Which direction do nevus cells move? Abtropfung reexamined. Am J Dermatopathol 1998;20:135-9.  Back to cited text no. 11
    
12.
Tokuda Y, Saida T, Murata H, Murase S, Oohara K. Histogenesis of congenital and acquired melanocytic nevi based on histological study of lesion size and thickness. J Dermatol 2010;37:1011-8.  Back to cited text no. 12
    
13.
Wang DG, Huang F, Chen W, Zhou Y, Wang CY, Zhu F, et al. Clinicopathological analysis of acquired melanocytic nevi and a preliminary study on the possible origin of nevus cells. Am J Dermatopathol 2019;42:1-9.  Back to cited text no. 13
    
14.
MacKie RM, English J, Aitchison TC, Fitzsimons CP, Wilson P. The number and distribution of benign pigmented moles (melanocytic naevi) in a healthy British population. Br J Dermatol 1985;113:167-74.  Back to cited text no. 14
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]



 

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